硼替唑咪治疗多发性骨髓瘤的分子机制  

The molecule mechanism of brotezomib in the treatment of multiple myeloma

作　　者：胡影[1] 陈世伦[1] 陈文明[1] 

机构地区：[1]首都医科大学附属北京朝阳医院血液科,100020

出　　处：《白血病．淋巴瘤》2007年第3期235-237,共3页Journal of Leukemia & Lymphoma

摘　　要：多发性骨髓瘤(MM)是一种恶性浆细胞肿瘤。造血干细胞移植将MM的中位生存期从传统化疗时的3年提高至5年,但仍无法治愈。近几年来沙利度胺(反应停)、砷剂、蛋白酶体抑制剂(硼替唑咪)等药物在MM的治疗中取得了较好的效果,特别是硼替唑咪治疗复发难治的MM的效果显著,治疗初发的MM的临床试验也正在进行中。对硼替唑咪治疗MM的作用机制及临床应用作一综述,期望为包括MM在内的血液系统恶性肿瘤的治疗提供依据。Multiple myeloma is a plasma cell malignancy.It's median survival has been elevated to 5 years from 3 years because of the use of hematological stem cell transplantation,but remains incurable.In recent years,thalidomide,arsenic trioxide,proteasome inhibitor(bortezomib) show the obvious effect in the treatment of multiple myeloma,especially bortezomib The review focuses on the action mechanism and clini- cal application of bortezomib in multiple myeloma in order to provide the evidence for the hematological ma- lignances.

关 键 词：多发性骨髓瘤 蛋白激酶抑制剂 分子作用机制 

分 类 号：R733.3[医药卫生—肿瘤]